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What is peritonitis? Peritonitis is an inflammation of the membrane which lines the inside of the abdomen and all of the internal organs known as the peritoneum.... THANK YOU and don't forget to SUBSCRIBE to our channel ITS EAZZY MED for you to get update on various tutorials that will help you master medicine quicky and easily . The information provided is for learning and should not substitute medical advice. THANK YOU.
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PARALYTIC ILEIUS causes,pathophysiology,clinical features,diagnosis and treatment
ILEUS also known as paralytic ileus is a temporary arrest of intestinal peristalsis. It occurs most commonly after abdominal surgery, particularly when the intestines have been manipulated. Symptoms are nausea, vomiting, and vague abdominal discomfort. Diagnosis is based on x-ray findings and clinical impression. Treatment is supportive, with nasogastric suction and IV fluids. Etiology In addition to postoperative causes, ileus also results from intraperitoneal or retroperitoneal inflammation (eg, appendicitis, diverticulitis, perforated duodenal ulcer), retroperitoneal or intra-abdominal hematomas (eg, ruptured abdominal aortic aneurysm, lumbar compression fracture), metabolic disturbances (eg, hypokalemia), or drugs (eg, opioids, anticholinergics, sometimes Ca channel blockers). Ileus sometimes occurs in association with renal or thoracic disease (eg, lower rib fractures, lower lobe pneumonias, MI). Gastric and colonic motility disturbances after abdominal surgery are common. The small bowel is typically least affected, with motility and absorption returning to normal within hours after surgery. Stomach emptying is usually impaired for about 24 h or more. The colon is often most affected and may remain inactive for 48 to 72 h or more. classic colicky pattern present in mechanical obstruction. There may be obstipation or passage of slight amounts of watery stool. Auscultation reveals a silent abdomen or minimal peristalsis. The abdomen is not tender unless the underlying cause is inflammatory. Diagnosis • Clinical evaluation • Sometimes x-rays The most essential task is to distinguish ileus from intestinal obstruction. In both conditions, x-rays show gaseous distention of isolated segments of intestine. In postoperative ileus, however, gas may accumulate more in the colon than in the small bowel. Postoperative accumulation of gas in the small bowel often implies development of a complication (eg, obstruction, peritonitis). In other types of ileus, xray findings are similar to obstruction; differentiation can be difficult unless clinical features clearly favor one or the other. Water-soluble contrast studies may help differentiate. Treatment • NGT • IV fluids Treatment involves continuous nasogastric suction, npo status, IV fluids and electrolytes, a minimal amount of sedatives, and avoidance of opioids and anticholinergic drugs. Maintaining an adequate serum K level (more than 4 mmol/L) is especially important. Ileus persisting more than 1 wk probably has a mechanical obstructive cause, and laparotomy should be considered. Sometimes colonic ileus can be relieved by colonoscopic decompression; rarely, cecostomy is required. Colonoscopic decompression is helpful in treating pseudo-obstruction (Ogilvie's syndrome), which consists of apparent obstruction at the splenic flexure, although no cause can be found by contrast enema or colonoscopy for the failure of gas and feces to pass this point. Some clinicians use IV neostigmine (requires cardiac monitoring) to treat Ogilvie's syndrome
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ENDOCARDITIS causes,symptoms,pathophysiology,diagnosis and treatment
Endocarditis (infective endocarditis) is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as vegetations, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify. There are several ways to classify endocarditis. The simplest classification is based on cause: either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu-like feeling, cardiac murmur, heart failure, petechia of anterior trunk, Janeway's lesions, Infective endocarditis is an infection of the inner surface of the heart, usually the valves. Symptoms may include fever, small areas of bleeding into the skin, heart murmur, feeling tired, and low red blood cells. Complications may include valvular insufficiency, heart failure, stroke, and kidney failure. The cause is typically a bacterial infection and less commonly a fungal infection. Risk factors include valvular heart disease including rheumatic disease, congenital heart disease, artificial valves, hemodialysis, intravenous drug use, and electronic pacemakers. The bacterial most commonly involved are streptococci or staphylococci. Diagnosis is suspected based on symptoms and supported by blood cultures or ultrasound.
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PHEOCHROMOCYTOMA causes,pathophysiology,clinical features,dx and treatment
PHEOCHROMOCYTOMA is a catecholamine secreting tumor of the adrenal gland originating from the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent. Extra-adrenal paragangliomas (often described as extra-adrenal pheochromocytomas) are closely related, though less common,
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FOURNIER GANGRENE causes,pathophysiology,features,diagnosis and treatment
Fournier gangrene, is a polymicrobial necrotizing fasciitis of the perineal, perianal, or genital areas Pathophysiology Localized infection adjacent to a portal of entry is the inciting event in the development of Fournier gangrene. Ultimately, an obliterative endarteritis develops, and the ensuing cutaneous and subcutaneous vascular necrosis leads to localized ischemia and further bacterial proliferation. Rates of fascial destruction as high as 2-3 cm/h have been described Signs & Symptoms Symptoms include fever, general discomfort (malaise), moderate to severe pain and swelling in the genital and anal areas (perineal) followed by rankness and smell of the affected tissues (fetid suppuration) leading to full blown (fulminating) gangrene. Rubbing the affected area yields the distinct sounds (crepitus) of gas in the wound and of tissues moving against one another (palpable crepitus). In severe cases, the death of tissue can extend to parts of the thighs, through the abdominal wall and up to the chest wall. This disease is commonly found in conjunction with other disorders (comorbidity), especially those that weaken the immune system. Some disorders that increase the predisposition to Fournier gangrene are diabetes mellitus, profound obesity, cirrhosis, interference with the blood supply to the pelvis, and various malignancies Causes Portals of entry for the bacteria, fungi, and/or viruses responsible for a particular case of Fournier gangrene are generally colorectal, urogenital or cutaneous in origin. Anorectal abscesses, urinary tract infections, surgical instrumentation and other contributing factors have all been implicated. Some cases continue to be of unknown cause (idiopathic). Why this process occasionally develops in individuals with common ailments is still not understood. There are many ways for the virulent microorganism to gain access to the host, where the compromised immunological system is unable to prevent the infection from taking hold. The virulence of the resulting disorder is thought to be enhanced by the toxins and enzymes produced by the combination of microorganisms (synergy).
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BRONCHIECTASIS etiology,pathophysiology,clinical features,diagnosis and treatment
Bronchiectasis is dilation and destruction of larger bronchi caused by chronic infection and inflammation. Common causes are cystic fibrosis, immune defects, and recurrent infections, though some cases seem to be idiopathic. Symptoms are chronic cough and purulent sputumexpectoration; some patients may also have fever and dyspnea. Diagnosis is based on history and imaging, usually involving high-resolution CT, though standard chest x-rays may be diagnostic. Treatment and prevention of acute exacerbations are with antibiotics, drainage of secretions, and management of complications, such as superinfection and hemoptysis. Treatment of underlying disorders is important whenever possible. Etiology Bronchiectasis may affect many areas of the lung (diffuse bronchiectasis), or it may appear in only one or two areas (focal bronchiectasis). Diffuse bronchiectasis develops in patients with genetic, immune, or anatomic defects that affect the airways. Cystic fibrosis is the most common cause. Immunodeficiencies may also cause diffuse disease, as may rare abnormalities in airway structure. Diffuse bronchiectasis is an uncommon complication of more common conditions, such as RAor Sjogren's syndrome. Allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to Aspergillus sp It occurs primarily in people with asthma and less commonly in people with cystic fibrosis and can lead to bronchiectasis. Focal bronchiectasis develops from untreated pneumonia or obstruction (eg, due to foreign bodies and tumors). Mycobacteria can cause focal bronchiectasis as well as colonize the lungs of patients with bronchiectasis due to other disorders Some cases have no readily apparent cause. Pathophysiology All the causative conditions impair airway clearance mechanisms and host defenses, resulting in an inability to clear secretions, which, in turn, predisposes patients to chronic infection and inflammation. As a result of frequent infections, most commonly with Haemophilus influenzae (35%), Pseudomonas aeruginosa (31%), Moraxella catarrhalis (20%), Staphylococcus aureus (14%), and Streptococcus pneumoniae (13%), airways become inspissated with viscous mucous containing inflammatory mediators and pathogens and slowly become dilated, scarred, and distorted. Histologically, bronchial walls are thickened by edema, inflammation, and neovascularization. Destruction of surrounding interstitium and alveoli causes fibrosis, emphysema, or both. Superinfection with multidrug-resistant organisms, including Mycobacterium tuberculosis, and mycobacteria other than M. tuberculosis can cause recurrent exacerbations and worsen airflow limitation on pulmonary function tests. Pulmonary hypertension and right-sided heart failure may ensue because functional lung tissue decreases. Symptoms and Signs Symptoms characteristically begin insidiously and gradually worsen over years. The major presenting symptom of bronchiectasis is chronic cough that almost always produces large volumes of thick, tenacious, purulent sputum. Dyspnea and wheezing are common. Hemoptysis, which can be massive, is due to neovascularization of the airways from the bronchial (as opposed to pulmonary) arteries. Acute exacerbations of disease due to new or worsened infection increase the extent of cough and the volume and purulence of sputum production. Low-grade fever may also be present and abnormal breath sounds, including crackles, rhonchi, and wheezing, are typical signs of disease. Finger clubbing may also be present. In advanced cases, hypoxemia and signs of pulmonary hypertension (eg, shortness of breath, dizziness) and right-sided heart failure can occur. Diagnosis • History and physical examination • Chest x-ray • High-resolution CT for confirmation • Pulmonary function tests for baseline function and progression of disease Treatment • Prevention of exacerbations with antibiotics and regular vaccinations • Measures to help clear secretions • Antibiotics for acute exacerbations • Sometimes surgical resection
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Kidney function tests are group of investigations done to evaluate the function of thr kidneys. They can be classified to two categories A. Tests for glomerular function B.Tests for tubular function The tests that are part of the Kidney Function test panel are: (a) Urine examination (b) Serum Urea (c) Serum creatinine (d) Blood urea nitrogen (BUN) (e) Calcium (f) Phosphorus (g) Protein (h) Albumin (i) Creatinine clearance (j) Urea clearance (k) Inulin clearance (l) Dilution and Concentration test (l) Serum electrolyte levels URINE EXAMINATION Before we do a quantitative examination of urine a qualitative examination is necessary as it can provide excellent clues to the nature and location of the lesion in the renal system. This examination consists of a physical examination where the colour, odour, quantity, specifc gravity etc of the urine is noted. Microscopic examination of urine is done to rule out any pus cells, Rbc casts, Crystals. SERUM UREA Urea is the end product of protein catabolism. The urea is produced from the amino group of the amino acids and is produced in the liver by means of the Urea cycle. BLOOD UREA NITROGEN (BUN) Sometimes the Serum urea level is expressed as blood urea nitrogen. BUN can be easily calculated from the serum urea level A rise in blood nitrogen level is known as azotemia. SERUM CREATININE LEVEL Creatine is a small tripeptide found in the muscles. It stays in its phosphorylated form and releases energy for any burst of muscular activity. It is released from the muscles during regular wear and tear and is converted to creatinine (its internal anhydride). It is to be remembered that unlike urea, creatinine is not a toxic waste. It is simply used as a marker of renal function. Creatinine is freely filtered at the glomerulus and is also to a very small extent secreted into the tubules. So any problem with gromerular filtrations has a significant effect on the excretion of creatinine resulting in a much substantial rise in serum creatinine level. Normal serum creatinine level is 0.6 to 1.5 mg/dl. Serum creatinine is a better indicator of renal function and more specifically glomerular function than urea. For a particular individual the creatinine level is dependent on the muscle mass and muscle wear and tear. There may be significant difference in creatinine level of individuals with vastly differing muscle mass. For example a body builder or athlete will have higher creatinine levels than a sedentary desk worker. Similarly creatinine level will also increase in case of any muscle trauma or excessive wear and tear as seems in athletes and people involved in hard physical labor. Creatinine is most commonly measured in laboratories calorimetrically by Jaffe’s method. UREA CLEARANCE Urea clearance is the hypothetical amount of blood from which kidney clears urea in one minute. This is measured by measuring the concentration of urea in blood, concentration of urea in urine and amount of urine excreted over a one hour interval. Urea clearance is less than its glomerular filtration as some of the urea that is filtered at the glomerulus is reabsorbed at the tubules. To measure urea clearance first the patient is made to void urine and then the made to drink two glasses of water. Then the urine is collected after an hour and a blood specimen is also collected at the same time. Then the patients urine sample is collected after another hour. The urea level in the two urine samples and the blood sample is measured. The urine volume is calculated as urine output per minute. The functional unit of the kidney is called a nephron. It consists of two main parts, the glomerulus and the tubular system. The glomerulus is composed of a bowman’s capsule and a tuft of leaky blood vessels encapsulated by the bowman’s capsule. The primary purpose of the glomerulus is filtrations. The leaky vessels filter into the glomerulus almost all the water, electrolytes, small proteins, nutrients such as sugar
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TOP 10 INCREDIBLE SELF SURGERIES (must watch for doctors)
Ever imagined of the feelings under the scalpel? or a surgeon cutting up himself? this video compilation is a MUST WATCH for all the medical doctors Self-surgery is the act of performing a surgical procedure on oneself. Sometimes it becomes necessity in extreme conditions to perform this act. This list includes 10 such individuals that because of great circumstances found it necessary to do so
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LEIOMYOMA (Fibroids)
What are leiomyomas? These are benign tumors that arise from the overgrowth of smooth muscle and connective tissue in the uterus...they are oestrogen dependent tumors that grow during the reproductive age
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What is Pierre Robin Sequence? Pierre Robin Sequence is a group of congenital malformations characterized by a triad of micrognathia, glossoptosis and U-shaped cleft palate.
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Myositis ossificans (MO) is a benign process characterised by heterotopic ossification usually within large muscles. Its importance stems in large part from its ability to mimic more aggressive pathological processes. Myositis ossificans is one of the skeletal “don’t touch” lesions. There are some conditions that are related to, or share similar name to, myositis ossificans  myositis ossificans circumscripta: refers to new bone that usually appears after trauma myositis ossificans progressiva: a rare, inherited disorder characterised by fibrosing and ossification of muscle, tendon and ligaments of multiple sites that are disabling and ultimately fatal panniculitis ossificans: similar to MO but occurring in subcutaneous tissues fibro-osseous pseudotumour of the digits: variant of MO occurring in the fingers and toes Pathology Myositis ossificans is essentially metaplasia of the intramuscular connective tissue resulting in extraosseous bone formation (without inflammation).  It has a zonal organisation  peripheral, well-organised mature lamellar bone intermediate osteoid region central immature non-ossified cellular (fibroblasts) focus Unfortunately, the histologically of myositis ossificans can appear similar to osteosarcoma, and thus, can lead to inappropriate management.
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MEN2 -is an autosomal dominant condition caused by mutation of the C-RET proto-oncogene The video describes MEN 2,causes,pathology,clinical manifestations,diagnosis and treatment
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NEPHROTIC SYNDROME causes,pathophysiology,diagnosis,features and treatment
Nephrotic syndrome is a collection of symptoms due to kidney damage. This includes (proteinuria) more than 3.5 g/day protein in the urine, low blood albumin levels (hypoalbuminemia), high blood lipids (hyperlipidemia) and significant swelling (edema) Other symptoms may include weight gain, feeling tired, and foamy urine. Complications may include blood clots (thrombosis), infections, and high blood pressure (hypertension). Causes include a number of kidney diseases such as focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease. It may also occur as a complication of diabetes or lupus. The underlying mechanism typically involves damage to the glomeruli of the kidney. Diagnosis is typically based on urine testing and sometimes a kidney biopsy. It differs from nephritic syndrome in that there are no red blood cells in the urine. Treatment is directed at the underlying cause. Other efforts include managing high blood pressure, high blood cholesterol, and infection risk. A low salt diet and limiting fluids is often recommended
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PATHOLOGY MNEMONICS Portal hypertension: features ABCDE: Ascites Bleeding (haematemesis, piles) Caput medusae Diminished liver Enlarged spleen Thrombosis and thrombocytopenia PARTNER together: Nephritic syndrome: glomerular diseases commonly presenting as nephritic syndrome Portal hypertension: features ABCDE: Ascites Bleeding (haematemesis, piles) Caput medusae Diminished liver Enlarged spleen Platelet count low Anemia (microangiopathic hemolytic) Renal failure Temperature rise Neurological deficits ER admission (as it is an emergency) MAKE PATHOLOGY SIMPLE AND FUN SUBSCRIBE TODAY
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PHENYTOIN: ADVERSE EFFECTS PHENYTOIN P-P-450 interactions H-Hirsutism E-Enlarged gums N-Nystagmus Y-Yellow-browning of skin T-Teratogenicity O-Osteomalacia I-Interference with B12 metabolism (hence anemia) N-Neuropathies: vertigo, ataxia, headache GYNAECOMASTIA-CAUSING DRUGS (DISCOS) D-Digoxin I-Isoniazid S-Spironolactone C-Cimetidine O-Oestrogens S-Stilboestrol K+ INCREASING AGENTS (K-BANK) K- K-sparing diuretic B- Beta blocker A- ACEI N- NSAID K- Ksupplement Amiodarone: action, side effects 6 P’s P-Prolongs action potential duration P-Photosensitivity P-Pigmentation of skin P-Peripheral neuropathy P-Pulmonary alveolitis and fibrosis P-Peripheral conversion of T4 to T3 is inhibited - hypothyroidis NICOTINIC EFFECTS (MTWTF) (DAYS OF WEEK): M-Mydriasis/ Muscle cramps T-Tachycardia W-Weakness T-Twitching H-Hypertension/ Hyperglycemia F-Fasiculation
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WHAT IS ZOLLINGER ELLISON SYNDROME? -It is a severe peptic ulceration of the stomach caused by a gastrin-secreting pancreatic islet non beta-cell tumour (‘gastrinoma’). -in this tutorial you shall learn about the pathology behind it, clinical manifestations, investigations and treatment.
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Hodgkins lymphoma is a neoplasm of the immune system that is marked by the presence of a type of cell called the Reed-Sternberg cell. The two major types of Hodgkin lymphoma are classical Hodgkin lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma. Classic Hodgkin lymphoma Classic Hodgkin lymphoma (cHL) accounts for more than 9 in 10 cases of Hodgkin lymphoma in developed countries. The cancer cells in cHL are called Reed-Sternberg cells. These cells are usually an abnormal type of B lymphocyte. Enlarged lymph nodes in people with cHL usually have a small number of Reed-Sternberg cells with a lot of normal immune cells around them. These other immune cells cause most of the swelling in the lymph nodes. Classic HL has 4 subtypes: nodular sclerosis Hodgkin lymphoma or NSCHL: This is the most common type of Hodgkin disease in developed countries. It accounts for about 7 out of 10 cases. It's most common in teens and young adults, but it can occur in people of any age. It tends to start in lymph nodes in the neck or chest. Mixed cellularity Hodgkin lymphoma or MCCHL: This is the second most common type, found in about 4 out 10 cases. It's seen mostly in people with HIV infection. It's also found in children or the elderly . It can start in any lymph node but most often occurs in the upper half of the body. Lymphocyte-rich Hodgkin lymphoma: This sub-type isn't common. It usually occurs in the upper half of the body and is rarely found in more than a few lymph nodes. Lymphocyte-depleted Hodgkin lymphoma: This is a rare form of Hodgkin disease. It's seen mainly in older people and those with HIV infection. It's more aggressive than other types of HL and likely to be advanced when first found. It's most often in lymph nodes in the abdomen (belly) as well as in the spleen, liver, and bone marrow. Nodular lymphocyte-predominant Hodgkin lymphoma Nodular lymphocyte-predominant Hodgkin lymphoma accounts for about 5% of cases. The cancer cells in NLPHL are large cells called popcorn cells (because they look like popcorn), which are variants of Reed-Sternberg cells. You may also hear these cells called lymphocytic and histiocytic (L&H) cells. NLPHL usually starts in lymph nodes in the neck and under the arm. It can occur in people of any age, and is more common in men than in women. This type of HL tends to grow more slowly and is treated differently from the classic types. Symptoms include the painless enlargement of lymph nodes, spleen, or other immune tissue. Other symptoms include fever, weight loss, fatigue, or night sweats. Also called Hodgkin disease.
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COOMBS TEST (antiglobulin test) made simple
Coombs test, as antiglobulin test or AGT is one of two tests used in immunohematology and immunology. The two Coombs tests are the direct Coombs test (DCT, also known as direct antiglobulin test or DAT), and the indirect Coombs test (also known as indirect antiglobulin test or IAT) The direct Coombs test is used to test for autoimmune hemolytic anemia In some conditions, an individual's blood may contain IgG antibodies that can specifically bind to antigens on the RBC surface membrane, and their circulating RBCs can become coated with IgG alloantibodies and/or IgG autoantibodies. Complement proteins may subsequently bind to the bound antibodies and cause RBC destructruction The direct Coombs test is used to detect the antibodies or complement proteins that are bound to the surface of red blood cells; a blood sample is taken and the RBCs are washed and then incubated with anti-human globulin "Coombs reagent". If this produces agglutination of RBCs, the direct Coombs test is positive, a visual indication that antibodies are bound to the surface of red blood cells. The indirect Coombs test is used in prenatal testing of pregnant women and in testing blood prior to a blood transfusion. It detects antibodies against RBCs that are present unbound in the patient's serum. In this case, serum is extracted from the blood sample taken from the patient. Then, the serum is incubated with RBCs of known antigenicity; that is, RBCs with known reference values from other patient blood samples. Finally, anti-human globulin is added. If agglutination occurs, the indirect Coombs test is positive
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1 know your study style "Learn how you learn". Make minimal changes to your study style and stick to it always 2 discipline is a must for a doctor to be.... 3.Prioritize your free time to most important things 4.Make time for yourself and your own wellbeing 5.Efficiency
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HEPATIC ENCEPHALOPATHY(portal systemic encephalopathy) causes,classification,features,dx and rx
HEPATIC ENCEPHALOPATHY (PORTAL-SYSTEMIC ENCEPHALOPATHY) Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. It most often results from high gut protein or acute metabolic stress (eg, GI bleeding, infection, electrolyte abnormality) in a patient with portal-systemic shunting As it progresses, confusion is followed by coma. Confusion needs to be differentiated from delirium tremens and Wernicke’s encephalopathy, and coma from subdural haematoma, which can occur in alcoholics after a fall Features include changes of intellect,personality, emotions and consciousness, with or without neurological signs Two broad categories of hepatic encephalopathy are covert (CHE) and overt (OHE) hepatic encephalopathy CHE is particularly associated with poor outcomes Hepatic encephalopathy is also classified into three types based on the disease state of the liver, as follows: Type A: Hepatic encephalopathy associated with acute liver failure Type B: Hepatic encephalopathy associated with portosystemic bypass with no intrinsic hepatocellular disease Type C: Hepatic encephalopathy associated with cirrhosis and portal hypertension or portosystemic shunts.
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DEXAMETHASONE SUPPRESSION TEST: How it is done and interpretation of the findings
The dexamethasone suppression test (DST) is a test that is used to assess the function of adrenal glands by measuring how cortisol levels change in response to an injection of dexamethasone. It is used to diagnose Cushing's syndrome.....
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DRUGS approved to treat erectile dysfunction are classified to three classes 1.PHOSPHODIESTEARASE 5INHIBITORS 2.VASODILATORS 3.ANDROGENS phosphodiestearase inhibitors include sildenafil
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ELECTROCARDIOGRAM waves and intervals explained
There are three main components to an ECG: the P wave, which represents the depolarization of the atria; the QRS complex, which represents the depolarization of the ventricles; and the T wave, which represents the repolarization of the ventricles.[6] It can also be further broken down into the following: O is the origin or datum point preceding the cycle P is the atrial systole contraction pulse Q is a downward deflection immediately preceding the ventricular contraction R is the peak of the ventricular contraction S is the downward deflection immediately after the ventricular contraction T is the recovery of the ventricles U is the successor of the T wave but it is small and not always observed During each heartbeat, a healthy heart has an orderly progression of depolarization that starts with pacemaker cells in the sinoatrial node, spreads throughout the atrium, passes through the atrioventricular node down into the bundle of His and into the Purkinje fibers, spreading down and to the left throughout the ventricles. This orderly pattern of depolarization gives rise to the characteristic ECG tracing. To the trained clinician, an ECG conveys a large amount of information about the structure of the heart and the function of its electrical conduction system. Among other things, an ECG can be used to measure the rate and rhythm of heartbeats, the size and position of the heart chambers, the presence of any damage to the heart's muscle cells or conduction system, the effects of heart drugs, and the function of implanted pacemakers
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brachial plexus
The brachial plexus is a network of nerves formed by the ventral rami of the lower four cervical nerves and first thoracic nerve (C5, C6, C7, C8, and T1). This plexus extends from the spinal cord, through the cervicoaxillary canal in the neck, over the first rib, and into the armpit. It supplies afferent and efferent nerve fibers to the chest, shoulder, arm and hand The brachial plexus is divided into five roots, three trunks, six divisions (three anterior and three posterior), three cords, and five branches. There are five "terminal" branches and numerous other "pre-terminal" or "collateral" branches, such as the subscapular nerve, the thoracodorsal nerve, and the long thoracic nerve, that leave the plexus at various points along its length. a common structure used to identify part of the brachial plexus in cadaver dissections is the M or W shape made by the musculocutaneous nerve, lateral cord, median nerve, medial cord, and ulnar nerve. Roots The five roots are the five anterior rami of the spinal nerves, after they have given off their segmental supply to the muscles of the neck. The brachial plexus emerges at five different levels; C5, C6, C7, C8, and T1. C5 and C6 merge to establish the upper trunk, C7 continuously forms the middle trunk, and C8 and T1 merge to establish the lower trunk. Prefixed or postfixed formations in some cases involve C4 or T2, respectively. The dorsal scapular nerve comes from the superior trunk and innervates the rhomboid muscles which retract the scapula. The subclavian nerve originates in both C5 and C6 and innervates the subclavius, a muscle that involves lifting the first ribs during respiration. The long thoracic nerve arises from C5, C6, and C7. This nerve innervates the serratus anterior, which draws the scapula laterally and is the prime mover in all forward-reaching and pushing actions. Trunks These roots merge to form the trunks: "superior" or "upper" (C5-C6) "middle" (C7) "inferior" or "lower" (C8, T1) Divisions Each trunk then splits in two, to form six divisions: anterior divisions of the upper, middle, and lower trunks posterior divisions of the upper, middle, and lower trunks when observing the body in the anatomical position, the anterior divisions are superficial to the posterior divisions Cords These six divisions regroup to become the three cords or large fiber bundles. The cords are named by their position with respect to the axillary artery. The posterior cord is formed from the three posterior divisions of the trunks (C5-C8, T1) The lateral cord is formed from the anterior divisions of the upper and middle trunks (C5-C7) The medial cord is simply a continuation of the anterior division of the lower trunk (C8, T1) Branches Most branch from the cords, but a few branch (indicated in italics) directly from earlier structures. The five on the left are considered "terminal branches". These terminal branches are the musculocutaneous nerve, the axillary nerve, the radial nerve, the median nerve, and the ulnar nerve. Due to both emerging from the lateral cord the musculocutaneous nerve and the median nerve are well connected. The musculocutaneous nerve has even been shown to send a branch to the median nerve further connecting them. There have been several variations reported in the branching pattern but these are very rare
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Adrenal glands are endocrine glands located on each kidney (suprarenal ) at a position of T10 and T11. They secrete hormones regulating metabolism (glucocorticoids), sexual function(androgens), water balance(mineralcorticoids) and stress hormones. They weigh about 4-6grams
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SHORT SYNACTHEN TEST (ACTH stimulation test) made simple
Standard Short Synacthen test for suspected adrenal failure Indication This is performed for the investigation of adrenal insufficiency. Contraindication The Synacthen test gives unreliable results within 2 weeks of pituitary surgery. Principle Adrenal glucocorticoid secretion is controlled by adrenocorticotrophic hormone (ACTH) released by the anterior pituitary. This test evaluates the ability of the adrenal cortex to produce cortisol after stimulation by synthetic ACTH (tetracosactide; Synacthen ). It does not test the whole pituitary-adrenal axis. The short test assesses the ability of the adrenal gland to respond to ACTH but is not reliable within 2 weeks of pituitary surgery. Preparation There are no dietary restrictions for this test. This test should be performed in the morning as the cortisol responses between the morning and late afternoon may differ by as much as 100 nmol/L at 30 min sample post Synacthen. Prednisolone should be stopped 24 hours before the Synacthen test. Requirements 2 plain tubes 250 microgram Synacthen (1 vial) the dose for children is 36 microgram/kg body weight up to a maximum of 250 micrograms Procedure 0900 take 3 mL blood for cortisol inject Synacthen iv or im 0930 take further sample for cortisol The above definition only defines adrenal insufficiency. The definition of normality is problematic since there is considerable variation in healthy individuals and a significant overlap with patients who have adrenal insufficiency. In ACTH deficiency the response to the short test may be normal or reduced. The response to Synacthen is not affected by obesity. There is no difference in cortisol response between iv & im administration. Baseline and incremental cortisol values do NOT apply to women taking oral contraceptives or to pregnant women. There is quite marked variation in the measurement of cortisol in the post-Syancthen samples by different laboratory methods Sensitivity and Specificity There are reports of patients with incipient adrenal failure with normal responses to Synacthen. The use of physiological doses eg 1 microgram may prove more useful at determining those subjects with poor responses than conventional (250 microgram) pharmacological doses. the standard test is better for diagnosing primary adrenal insufficiency. However, whilst there is no difference in diagnostic performance between the standard and low dose tests in cases of secondary adrenal insufficiency, neither test is recommended where there is a possibility of pituitary dysfunction
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CIRRHOSIS (causes,pathophysiology,features,diagnosis,treatment)
Cirrhosis is defined as the presence of fibrous bands that divide the liver into regenerative nodules. Cirrhosis represents a late stage of progressive hepatic fibrosis MERCK MANUAL Professional Version Tap to switch to the Consumer Version ShareEmailLinkedInFacebookGoogle+Twitter Cirrhosis By Jesse M. Civan, MD, Assistant Professor and Medical Director, Liver Tumor Center, Thomas Jefferson University Hospital CLICK HERE FOR Patient Education Cirrhosis is a late stage of hepatic fibrosis that has resulted in widespread distortion of normal hepatic architecture. Cirrhosis is characterized by regenerative nodules surrounded by dense fibrotic tissue. Symptoms may not develop for years and are often nonspecific (eg, anorexia, fatigue, weight loss). Late manifestations include portal hypertension, ascites, and, when decompensation occurs, liver failure. Diagnosis often requires liver biopsy. Cirrhosis is usually considered irreversible. Treatment is supportive. Cirrhosis is a leading cause of death worldwide. The causes of cirrhosis are the same as those of fibrosis (see Table: Disorders and Drugs That Can Cause Hepatic Fibrosis). In developed countries, most cases result from chronic alcohol abuse or chronic hepatitis C. In parts of Asia and Africa, cirrhosis often results from chronic hepatitis B. (See table: Characteristics of Hepatitis Viruses for additional information on hepatitis B and C.) Cirrhosis of unknown etiology (cryptogenic cirrhosis) is becoming less common as many specific causes (eg, chronic hepatitis C, steatohepatitis) are identified. Injury to the bile ducts also can result in cirrhosis, as occurs in mechanical bile duct obstruction, primary biliary cholangitis, and primary sclerosing cholangitis. Pathophysiology There are 2 primary ingredients: Hepatic fibrosis Regenerating liver cells In response to injury and loss, growth regulators induce hepatocellular hyperplasia (producing regenerating nodules) and arterial growth (angiogenesis). Among the growth regulators are cytokines and hepatic growth factors (eg, epithelial growth factor, hepatocyte growth factor, transforming growth factor-alpha, tumor necrosis factor). Insulin, glucagon, and patterns of intrahepatic blood flow determine how and where nodules develop Angiogenesis produces new vessels within the fibrous sheath that surrounds nodules. These vessels connect the hepatic artery and portal vein to hepatic venules, restoring the intrahepatic circulatory pathways. Such interconnecting vessels provide relatively low-volume, high-pressure venous drainage that cannot accommodate as much blood volume as normal. As a result, portal vein pressure increases. Such distortions in blood flow contribute to portal hypertension, which increases because the regenerating nodules compress hepatic venules. The progression rate from fibrosis to cirrhosis and the morphology of cirrhosis vary from person to person. Presumably, the reason for such variation is the extent of exposure to the injurious stimulus and the individual’s response. It is a histological diagnosis and can be classified into micro and macronodular by the size of mm. Risk of developing Hepatocellular Carcinoma Chronic Viral Infection - HBV HCV Wilson's disease α-1 antitrypsin deficiency Alcohol Haemochromatosis NASH Alcohol and liver Steatosis - is reversible with alcohol abstention Alcoholic hepatitis - Mallory body Alcoholic cirrhosis - hobnail appearance Causes Chronic Hepatitis C infection (Alcoholic liver disease (AST more than ALT Elevated GGT) Chronic Hepatitis B infection (HBsAg HBeAg/HBV-DNA) Autoimmune liver disease (Raised Ig and Autoantibodies) Primary Sclerosing cholangitis (pANCA MRCP/ERCP) Primary Biliary cirrhosis (Anti Mitochondrial Ab) Hereditary Haemochromatosis (Ferritin high Transferrin saturation high, Genetics) Wilson's disease (Young, low Ceruloplasmin raised Urine copper, KF rings) Budd-Chiari syndrome (USS caudate lobe) Drugs - amiodarone, methotrexate, methyldopa Cystic fibrosis (genetics + sweat Cl) Alpha-1 antitrypsin (Young emphysema low serum AAT) Idiopathic - unknown Drugs that should be avoided in Cirrhosis These would include NSAIDs with their effects on kidneys and gastric mucosa. ACE inhibitors may be involved in hepatorenal syndrome and are best stopped. Codeine, Narcotics, Benzodiazepines and anxiolytics can all precipitate or worsen hepatic encephalopathy Complications Portal hypertension Liver failure Portosystemic Encephalopathy - always look for flap and assess mental state Variceal Bleeding formed from left gastric and short gastric veins to the oesophagus Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Osteoporosis Hepatocellular carcinoma Investigations U&E LFT's (low Na common) Prothrombin time and Albumin reflect liver synthetic functi
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CUSHING SYNDROME causes,pathophysiology,features,dx and treatment
Cushing’s syndrome results from excess cortisol secretion from adrenal adenoma and excessive activation of glucocorticoid receptors. It can be: Iatrogenic, due to prolonged administration of synthetic glucocorticoids such as prednisolone. Endogenous due to chronic over-production of cortisol by the adrenal glands, either as the result of an adrenal tumour or because of excessive production of ACTH by a pituitary tumour or ectopic ACTH production by other tumours. EPIDEMIOLOGY Male to female incidence ratio is 5:1 of cushing syndrome due to pituitary or adrenal tumor Ectopic ACTH production is more common in males than females because of higher incidence of lung tumors in men Peak incidence of cushing syndrome due to either adrenal or pituitary adenoma is in persons aged 25-40 years Ectopic ACTH production occurs in later life AETIOLOGY  ACTH DEPENDENT CUSHING SYNDROME -primary adrenal lesions A.Adrenal adenoma B.Adrenal carcinoma C.Macronodular or micronodular adrenal hyperplasia D. McCune-Albright syndrome -ectopic cortisol secretion from a case of ovarian carcinoma   ACTH INDEPENDENT CUSHING SYNDROME -ACTH producing pituitary adenoma Nelson syndrome -small cell lung carcinoma cause ectopic ACTH secretionAmongst endogenous causes, pituitary-dependent cortisol excess (byconvention, called Cushing’s disease) accounts for approximately 80% of cases. -Pseudo cushing can be due to hypercortisolism due to the following -Alcoholism -Depression -Obesity clinical features -Hair thinning -Acne plethora -Moon face -Hyperglycemia -Loss of height and back pain -Menstrual disturbance -Psychosis -Cataracts -Hypertension -Osteoporosis -hypokalemia Hypercalciuria Bufallo humps and truncal obesity -Decreased skin tickhness -Wasting and weakening of proximal thigh and extremities muscles(proteolysis) -Mild exophthalmos -Tendency to infections(immune suppression by inhibiting histamine release,intereukins and phospolipase A2) - poor wound healing -bruising -weight increase -metabolic alkalosis -hirsutism -striae(impared collagen synthesis)   Cushing disease is caused by a benign monoclonal pituitary corticotroph adenoma that secretes excess ACTH which in turn causes supraphysiological secretion of glucocorticoids from the adrenal glands. the excess circulating cortisol disrupts normal physiologic dunal variationin the cortisol levels and excerts a negative feedback inhibition on corticotrophin releasing hormone secretion from the hypothalamus. However the adenoma itself is resistant to inhibition by endogenous circulating cortisol. Consequently cushing disease is associated with suppressed secretion of CRH and elevated levels of ACTH in relation to the degree of cortisol production.   Endogenous excess cortisol overproduction that is independent of ACTH is usually due to an adenoma and rarely a carcinoma. . Ectopic cortisol secretion from a case of ovarian carcinoma is a cause of ACTH-independent Cushing syndrome. ACTH level in ACTH-independent Cushing syndrome is low due to the negative feedback to pituitary corticotroph cells from a high level of serum cortisol. ACTH-dependent Cushing syndrome is characterized by elevated ACTH levels. Elevated ACTH levels are usually due to an anterior pituitary tumor, which is classic Cushing disease Nonpituitary ectopic sources of ACTH, such as small-cell lung carcinoma , carcinoid tumor, medullary thyroid carcinoma, or other neuroendocrine tumors can result in high ACTH levels and sequentially hypercortisolism Ectopic corticotropin-releasing hormone (CRH) secretion leading to increased ACTH secretion comprises a very rare group of cases of Cushing syndrome Low dose dexamethasone suppression test (1 mg at 12 midnight and test serum cortisol the next day at 8 am) to differentiate btn cushing syndrome from pseudo cushing syndrome…in cushing cortisol level drops 24 hr urinary cortisol or serum cortisol at 8 am- in true syndrome levels will increase ACTH levels increases in pituitary adenoma and ectopic tumor but reduced in adrenal adenoma High dose dexamethasone suppression test to differentiate between pituitary adenoma and ectopic tumour) ACTH and cortisol levels remain high in ectopic but reduces in pituitary adenoma to locate the pituitary adenoma go for MRI but it isn’t confirmatory. Most accurate test to dx cushing disease is inferior petrosal sinus blood sample ACTH level . It the ACTH level in IPS/peripheral blood is more than 2 then its confirmatory TREATMENT AND MANAGEMENT The treatment for endogenous cushing syndrome is the removal of the pituitary, ectopic (usually in lung) or adrenal tumour if possible, coupled with corticosteroid replacement therapy. The primary therapy for cushing disease is transphenoidal surgery by an experienced neurosurgeon and the primary therapy for adrenal tumors is adrenalectomy Pituitary radiation therapy is useful if surgery fails to resolve the problem.Normalization of cormobidities
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Hypothyroidism is also known as underactive thyroid. It is a condition in which the thyroid gland produces an abnormally low amount of thyroid hormone The disorder can be classified to three PRIMARY THYROIDISM SECONDARY HYPOTHYROIDISM TRANSIENT HYPOTHYROIDISM
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WHAT IS PULMONARY HYPERTENTION? Pulmonary hypertension is a lung condition in which there is increased pressure in the pulmonary arteries that travel from the heart to the lungs...ITS DEFINED as It is a mean pulmonary artery pressure of more than 25 mmHg at rest.... SUBSCRIBE and follow us on our youtube channel for more tutorials to aid in your revision. thank you ITS EAZZY MED
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WHAT IS ENDOMETRIAL CARCINOMA? endometrial carcinoma is a malignancy that arises from endometrial hyperplasia..... In this tutorial you shall learn on the subtypes, risk factors,clinical features, pathology , diagnosis and treatment approaches.
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OSTEOMYELITIS causes,pathophysiology,classification,clinical features,diagnosis and treatment
Osteomyelitis is inflammation of the bone and the bone marrow caused by an infecting organism. Although bone is normally resistant to bacterial colonization, events such as trauma, surgery, the presence of foreign bodies, or the placement of prostheses may disrupt bony integrity and lead to the onset of bone infection. Osteomyelitis can also result from hematogenous spread after bacteremia. When prosthetic joints are associated with infection, microorganisms typically grow in biofilm, which protects bacteria from antimicrobial treatment and the host immune response. Early and specific treatment is important in osteomyelitis, and identification of the causative microorganisms is essential for antibiotic therapy. The major cause of bone infections is Staphylococcus aureus. Infections with an open fracture or associated with joint prostheses and trauma often must be treated with a combination of antimicrobial agents and surgery. When biofilm microorganisms are involved, as in joint prostheses, a combination of rifampin with other antibiotics might be necessary for treatment.
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Appendicitis is an acute inflamation and infection of the vermiform appendix... in this video we will discuss the causes,pathology, signs and symptoms of appendicitis, Alvaro score , diagnostic tests and treatment.
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The oral glucose tolerance test (OGTT) was the gold standard for making the diagnosis oftype 2 diabetes. It is still commonly used during pregnancy for diagnosing gestational diabetes. With an oral glucose tolerance test, the person fasts overnight (at least 8 hours, but not more than 16 hours). The next morning, the fasting plasma glucose is tested. After this test, the person receives a dose of oral glucose (the dose depends upon the length of the test). There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken up to four times at different time points after consumption of the sugar to measure the blood glucosethe illustration describes what is glucose tolerance test? why is glucose tolerance test done? how it is done and how the results are interpretted.
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Liver function tests (LFTs or LFs) refers to a battery of blood tests that give information about the state of a patient's liver. USES Screening : They are a non-invasive yet sensitive screening modality for liver dysfunction. Pattern of disease : They are helpful to recognize the pattern of liver disease. Like being helpful in differentiating between acute viral hepatitis and various cholestatic disorders and chronic liver disease. (CLD). Assess severity : They are helpful to assess the severity and predict the outcome of certain diseases like primary biliary cirrhosis. Follow up : They are helpful in the follow up of certain liver diseases and also helpful in evaluating response to therapy like autoimmune hepatitis. LIMITATIONS Lack sensitivity: The LFT may be normal in certain liver diseases like cirrhosis, non cirrhotic portal fibrosis, congenital hepatic fibrosis, Lack specificity : They lack specificity and are not specific for any particular disease. Serum albumin may be decreased in chronic disease and also in nephrotic syndrome. Aminotransferases may be raised in cardiac diseases and hepatic diseases. Except for serum bile acids the LFT are not specific for liver diseases and all the parameters may be elevated for pathological processes outside the liver. Thus, we see that LFT have certain advantages as well as limitations at the same time. Thus, it is important to view them keeping the clinical profile of the patient in mind. CLASSIFICATION OF LIVER FUNCTION TESTS A. Tests of the liver’s capacity to transport organic anions and to metabolize drugs- Serum bilirubin, urine bilirubin, urobilinogen B. Tests that detect injury to hepatocytes (serum enzyme tests) – Aminotransferases, alkaline phosphatase, ã glutamyl transpeptidase, 5 nucleotidase, leucine aminopeptidase C. Tests of the Liver’s biosynthetic capacity- Serum proteins, albumin, prealbumin, serum ceruloplasmin, procollagen III peptide, a 1 antitrypsin, a feto protein, prothrombin time etc. Tests of the liver’s capacity to transport organic anions and to metabolize drugs These tests include prothrombin time (PT/INR), aPTT, albumin, bilirubin (direct and indirect), and others. The liver transaminases aspartate transaminase (AST or SGOT) and alanine transaminase (ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function. Most liver diseases cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance. This testing is performed on a patient's blood sample. Some tests are associated with functionality (e.g., albumin), some with cellular integrity (e.g., transaminase), and some with conditions linked to the biliary tract (gamma-glutamyl transferase and alkaline phosphatase). Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to detect the presence of liver disease, distinguish among different types of liver disorders, gauge the extent of known liver damage, and follow the response to treatment.
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WHAT IS POLYCYSTIC OVARIAN SYNDROME? Polycystic ovary syndrome (PCOS) is a set of symptoms due to elevated androgens (male hormones) in females. Signs and symptoms of PCOS include: signs of anovulation such as amenorrhea ,oligomenorrhea, excess body and facial hair... in this video you will learn of its pathophysiologyy, risk factors , clinical features,diagnosis and management....
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CROHN'S DISEASE causes,pathophysiology,clinical features,diagnosis and treatment
Crohn's disease is an inflammatory bowel disease (IBD). It causes inflammation of your digestive tract, which can lead to abdominal pain, severe diarrhea, fatigue, weight loss and malnutrition. Inflammation caused by Crohn's disease can involve different areas of the digestive tract in different people
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Cells require oxygen from the air to extract energy from glucose through respiration, which produces carbon dioxide and water as a waste product. Therefore, oxygen is vital for every part of normal cellular function, and oxygen deficiency can have severe pathological consequences. The respiratory system facilitates breathing. In the alveoli tissue of the lungs, the exchange of oxygen and carbon dioxide molecules between the air and the bloodstream occurs by passive transport, so that oxygen is taken in and carbon dioxide and water are removed. Passive diffusion (also called bulk flow) is the term for the movement of these gases between the air and bloodstream based on their relative concentration, with the gas with the greater concentration moving across to the area with the lower concentration. This process consumes no energy. The circulatory system is deeply connected with the respiratory system because it distributes the dissolved oxygen to the tissues of the body and the waste carbon dioxide to the lungs. The primary function of the respiratory system is gas exchange between the external environment and an organism’s circulatory system. In humans and other mammals, this exchange balances oxygenation of the blood with the removal of carbon dioxide and other metabolic wastes from the circulation. It shows a cutaway view of the pulmonary alveoli as the terminal ends of the respiratory tree, outcropping from either alveolar sacs or alveolar ducts, which are both sites of gas exchange with the blood. Bronchial anatomy: The pulmonary alveoli are the terminal ends of the respiratory tree, outcropping from either alveolar sacs or alveolar ducts, which are both sites of gas exchange with the blood. As gas exchange occurs, the acid-base balance of the body is maintained as part of homeostasis. If proper ventilation is not maintained, two opposing conditions could occur: respiratory acidosis (a life threatening condition) and respiratory alkalosis. At the molecular level, gas exchange occurs in the alveoli—tiny sacs which are the basic functional component of the lungs. The alveolar epithelial tissue is extremely thin and permeable, allowing for gas exchange between the air inside the lungs and the capillaries of the blood stream. Air moves according to pressure differences, in which air flows from areas of high pressure to areas of low pressure.
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ANAEMIA causes,classification,clinical features,treatment
Anaemia is a decrease in the RBC count, HGB and/or HCT values as compared to normal reference range for age and sex. Functionally defined as the inability of haemoglobin to supply the tissues with adequate oxygen.....hypoxia. ‘True’ anemia….decreased RBC mass and normal plasma volume. Pseudo or dilutional anemia….normal RBC mass and increased plasma volume . An increase in plasma volume may cause a dilutional or pseudo anemia (with low Hgb & HCT values) even though the RBC mass is normal ....can occur during pregnancy or caused by volume overload (IVs), congestive heart failure. 1. Classification of Anemia I. Etiologic Classification • Impaired RBC production • Excessive destruction • Blood loss II. Morphologic Classification • Macrocytic anemia • Microcytic hypochromic anemia • Normochromic normocytic anemia 2. Impaired RBC Production 1. Abnormal bone marrow • Aplastic anemia • Myelophthisis : Myelofibrosis, Leukemia, Cancer metastasis 2. Essential factors deficiency • Deficiency anemia : Fe, Vit. B12, Folic acid, etc • Anemia in renal disease : Erythropoietin 3. Stimulation factor deficiency • Anemia in chronic disease • Anemia in hypopituitarism • Anemia in hypothyroidism 3. Excessive Destruction of RBC Hemolytic anemia Intracorpuscular defect ;- • Membrane : Hereditary spherocytosis Hereditary ovalocytosis, etc. • Enzyme : G-6PD deficiency, PK def., etc. • Hemoglobin : Thalassemia, Hemoglobinopathies Extracorpuscular defect • Mechanical : March hemolytic anemia MAHA (Microangiopathic HA) • Chemical/Physical • Infection : Clostridium tetani • Antibodies : HTR, SLE • Hypersplenism Blood Loss • Acute blood loss : Accident, GI bleeding • Chronic blood loss : Hypermenorrhea, Parasitic infestation II. Morphologic Classification Macrocytic AnemiaMegaloblastic dyspoiesis • Vit. B12 deficiency: Pernicious anemia • Folic acid deficiency: Nutritional megaloblastic anemia, Sprue, Other malabsorption • Inborn errors of metabolism: Orotic aciduria, etc. • Abnormal DNA synthesis: Chemotherapy, Anticonvulsant, Oral contraceptives Microcytic Hypochromic AnemiaFe deficiency anemia: Chronic blood loss, Inadequate diet, Malabsorption, Increased demand, etc. • Abnormal globin synthesis: Thalassemia with or without Hemoglobinopathies • Abnormal porphyrin and heme synthesis: Pyridoxine responsive anemia, etc. • Other abnormal Fe metabolism: Normocytic Normochromic Anemia Blood loss • Increased plasma volume: Pregnancy, Overhydration • Hemolytic anemia: depend on each cause • Hypoplastic marrow: Aplastic anemia, RBC aplasia • Infiltrate BM: Leukemia, Multiple myeloma, Myelofibrosis, etc. • Abnormal endocrine: Hypothyroidism, Adrenal insufficiency, etc. • Kidney disease/Liver disease/Cirrhosis Hemolytic Anemia What is Hemolysis • Premature destruction of red cells. • Caused by hereditary and acquired disorders. Hemolysis occurs at two sites: Intravascular • Hemolysis occurs within systemic circulation. • Hemoglobin is released into plasma. • Hemoglobin is lost through kidneys or catabolized in the liver. Extravascular • Trapping of red cells in spleen or liver sinuses. • Lyses of trapped red cells. • Release of lysed hemoglobin and catabolism within the sequestering organ. Classification of Hereditary Hemolytic Anemia • Based on side effect: • Metabolic defect • Membrane defect • Hemoglobin defect A) Metabolic defect: • Defect in hexose monophosphate shunt: G-6-PD deficiency. • Defects of glycolysis: pyruvate kinase def., glucose phosphate isomerase deficiency. • Defects in red cell nucleotide metabolism: pyrimidine-5-nucleotidase def. B) Membrane defect: • Hereditary spherocytosis • Hereditary elliptocytosis • Hereditary pyropoikilocytosis C) Hemoglobin defect:  Thalassemias  Sickle cell anemia  Hemoglobin C disease  Hemoglobin E disease  Unstable hemoglobin
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HEMOSTASIS (blood clotting process, clotting factors,regulation and anticoagulants
Hemostasis is the natural process that stops blood loss when an injury occurs.It involves three steps: (1) vascular spasm ( vasoconstriction ); (2) platelet plug formation; and (3) coagulation. Vasoconstriction is a reflex in which blood vessels narrow to increase blood pressure. Next, platelet plug formation involves the activation, aggregation, and adherence of platelets into a plug that serves as a barrier against blood flow. Coagulation involves a complex cascade in which a fibrin mesh is cleaved from fibrinogen. Fibrin acts as a “molecular glue” during clot formation, holding the platelet plug together. Steps of Hemostasis Hemostasis includes three steps that occur in a rapid sequence: (1) vascular spasm, or vasoconstriction, a brief and intense contraction of blood vessels; (2) formation of a platelet plug; and (3) blood clotting or coagulation, which reinforces the platelet plug with fibrin mesh that acts as a glue to hold the clot together. Once blood flow has ceased, tissue repair can begin. Vasoconstriction Intact blood vessels are central to moderating blood’s clotting tendency. The endothelial cells of intact vessels prevent clotting by expressing a fibrinolytic heparin molecule and thrombomodulin, which prevents platelet aggregation and stops the coagulation cascade with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which causes platelet adherence during the initial formation of a clot. The vasoconstriction that occurs during hemostasis is a brief reflexive contraction that causes a decrease in blood flow to the area. Platelet Plug Formation Platelets create the “platelet plug” that forms almost directly after a blood vessel has been ruptured. Within twenty seconds of an injury in which the blood vessel’s epithelial wall is disrupted, coagulation is initiated. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes, the platelet plug is completely formed by fibrin. Contrary to popular belief, clotting of a skin injury is not caused by exposure to air, but by platelets adhering to and being activated by collagen in the blood vessels’ endothelium. The activated platelets then release the contents of their granules, which contain a variety of substances that stimulate further platelet activation and enhance the hemostatic process. When the lining of a blood vessel breaks and endothelial cells are damaged, revealing subendothelial collagen proteins from the extracellular matrix, thromboxane causes platelets to swell, grow filaments, and start clumping together, or aggregating. Von Willebrand factor causes them to adhere to each other and the walls of the vessel. This continues as more platelets congregate and undergo these same transformations. This process results in a platelet plug that seals the injured area. If the injury is small, the platelet plug may be able to form within several seconds. Coagulation Cascade If the platelet plug is not enough to stop the bleeding, the third stage of hemostasis begins: the formation of a blood clot. Platelets contain secretory granules. When they stick to the proteins in the vessel walls, they degranulate, thus releasing their products, which include ADP (adenosine diphosphate), serotonin, and thromboxane A2 (which activates other platelets). First, blood changes from a liquid to a gel. At least 12 substances called clotting factors or tissue factors take part in a cascade of chemical reactions that eventually create a mesh of fibrin within the blood. Each of the clotting factors has a very specific function. Prothrombin, thrombin, and fibrinogen are the main factors involved in the outcome of the coagulation cascade. Prothrombin and fibrinogen are proteins that are produced and deposited in the blood by the liver. When blood vessels are damaged, vessels and nearby platelets are stimulated to release a substance called prothrombin activator, which in turn activates the conversion of prothrombin, a plasma protein, into an enzyme called thrombin. This reaction requires calcium ions. Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long, insoluble fibers or threads of the protein, fibrin. Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot. This net of fibers traps and helps hold platelets, blood cells, and other molecules tight to the site of injury, functioning as the initial clot. This temporary fibrin clot can form in less than a minute and slows blood flow before platelets attach. Next, platelets in the clot begin to shrink, tightening the clot and drawing together the vessel walls to initiate the process of wound healing.
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The pancreas is a 6 inch-long glandthat is located in retroperitoneum near the liver and part of the small intestine. It has both an endocrine and exocrine function. Endocrine function the pancreas secretes hormones, including the blood sugar-regulating hormones: insulin and glucagon. Exocrine function of the pancreas involves secretion of enzymes that help break down substances for proper digestion and absorption. In this video we shall look at its endrocrine function
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DRUGS OF CHOICE -(Disease -drug correlation guide)
Drugs of choice for various conditions 1. Enuresis = imipramine 2. Rheumatic fever =penicillin 3. Paracetamol poisoning- :- - acetyl cysteine 4. acute bronchial- asthma :- salbutamol 5. acute gout :- NSAIDS 6. acute hyperkalemia:- calcium gluconate 7. severe DIGITALIS toxicity :-DIGIBIND 8. acute migraine :- sumatriptan 9. cheese reaction :- phentolamine 10. atropine poisoning :- physostigmine 11. cyanide poisoning :- amyl nitrite 12. benzodiazepine poisoning:- flumazenil 13. cholera :- tetracycline 14. KALA-AZAR :- lipozomal amphotericin- B 15. iron poisoning :- desferrioxamine 16. MRSA :- vancomycin 17. VRSA :- LINEZOLID 18. warfarin overdose :- vitamin-K (NIPER- 2009) 19. OCD - fluoxetine 20. alcohol poisoning :- fomepizole 21. epilepsy in pregnency :- phenobarbitone 22. anaphylactic shock :- Adrenaline 23. Malaria in Pregnancy-Chloroquine 24. Whooping Cough or Perteusis- Erythromycin 25. Kawasaki disease-IV Ig 26. Heparin Overdose-Protamine 27. Hairy Cell Leukemia-Cladirabine 28. Multiple Myeloma- Melphalan 29. CML-Imatinib 30. Wegner's granulomatosis-Cyclophosphamide 31. HOCM- Propranolol 32. Delirium Tremens-Diazepam 33. Drug Induced Parkinsonism-Benzhexol 34. Diacumarol Poisoning-Vit-K 35. Type-1 Lepra Reaction-Steroids 36. Type- 2 Lepra Reaction-Thalidomide 37. Allergic Contect Dermatitis-Steroids 38. PSVT- 1st-Adenosine, 2nd-Verapamil, 3rd-Digoxin 39. Z-E Syndrome- Proton Pump Inhibitor 40. Chancroid-Cotrimoxazole 41. Dermatitis Herpetiformis-Dapsone 42. Spastic Type of Cerebral Palsy-Diazepam 43. Herpis Simplex Keratitis-Trifluridine 44. Herpes Simplex Orolabialis-Pancyclovir 45. Neonatal Herpes Simplex-Acyclovir 46. Pneumocystis carinii Pneumonia- 47. Cotrimoxazole - Nodulo . 48. Trigeminal Neuralgia-Carbamezapine 49. Actinomycosis-Penicillin 50. Plague- Streptomycin 51. Opioid Withdrawal- Methadone 2nd-Clonidine 52. Alcohol Withdrawal- Chlordiazepoxide 2nd Diazepam 53. Post Herpetic Neuralgia- Fluphenazine 54. WEST Syndrome-ACTH 55. Diabetic Diarrhoea- Clonidine 56. Lithium Induced Neuropathy-Amiloride Communicable Disease: 57. Tetanus: PEN G Na; TETRACYCLINE; (DIAZEPAM 58. Diphteria: PEN G K; ERYTHROMYCIN 59. Pertusis: ERYTHROMYCIN; AMPICILLIN 60. Meningitis: MANNITOL (osmotic diuretic); DEXAMETHASONE (anti-inflammatory); DILANTIN/PHENYTOIN (anti-convulsive); PYRETINOL/ENCEPHABO L (CNS stimulant) 61. Amoebic Dysentery: METRONIDAZOLE 62. Shigellosis: CO-TRIMOXAZOLE 63. Typhoid: CHLORAMPHENICOL 64. Rabies: LYSSAVAC, VERORAB 65. Immunoglobulins: ERIG or HRIg 66. Malaria: CHLOROQUINE 67. Schistosomiasis: PRAZIQUANTEL 68. Felariasis: DIETHYLCARBAMAZINE CITRATE 69. Scabies: EURAX/ CROTAMITON 70. Chicken pox: ACYCLOVIR/ZOVIRAX 71. Leptospirosis: PENICILLIN; TETRACYCLINE; ERYTHROMYCIN 72. Leprosy: DAPSONE, RIFAMPICIN 73. Anthrax: PENICILLIN 74. Tuberculosis: R.I.P.E.S. 75. Pneumonia: COTRIMOXAZOLE; Procaine Penicillin 76. Helminths: MEBENDAZOLE; PYRANTEL PAMOATE 77. Syphilis: PENICILLIN 78. Gonorrhea: PENICILLIN 79. Cystic Acne -Retinoic aciddrug of choice -Retinoic
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HEMORRHOIDS causes,types,clinical features,diagnosis and treatment
Hemorrhoids are swollen veins located around the anus or in the lower rectum. About 50 percent of adults experienced the symptoms of hemorrhoids by the age of 50. Hemorrhoids can either be internal or external. Internal hemorrhoids develop within the anus or rectum. External hemorrhoids develop outside of the anus. Hemorrhoids are also known as piles. External hemorrhoids are the most common and most troublesome. Hemorrhoids cause pain, severe itching, and difficulty sitting. Fortunately, they are treatable
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BENIGN PROSTATIC HYPERTROPHY (BPH) pathology,features,diagnosis and treatment
Benign prostatic hyperplasia, a noncancerous enlargement of the prostate gland, is the most common benign tumor found in men. BPH produces symptoms by obstructing the flow of urine through the urethra. Symptoms related to BPH are present in about one in four men by age 55, and in half of 75-year-old men. However, treatment is only necessary if symptoms become bothersome. By age 80, some 20 to 30% of men experience BPH symptoms severe enough to require treatment. Surgery was the only option until the recent approval of drugs that can relieve symptoms either by shrinking the prostate or by relaxing the prostate muscle tissue that constricts the urethra. Diagram of an enlarged prostate gland, showing the prostate gland compressing the urethra and blocking the flow of urine from the bladder Signs and Symptoms The symptoms of BPH can be divided into those caused directly by urethral obstruction and those due to secondary changes in the bladder. Typical obstructive symptoms are: Difficulty in starting to urinate despite pushing and straining A weak stream of urine; several interruptions in the stream Dribbling at the end of urination Bladder changes cause: A sudden strong desire to urinate (urgency) Frequent urination The sensation that the bladder is not empty after urination is completed Frequent awakening at night to urinate (nocturia) As the bladder becomes more sensitive to retained urine, a man, may become incontinent (unable to control the bladder causing bed wetting at night, or inability to respond quickly enough to urinary urgency). Burning or pain during urination can occur if a bladder infection or stone is present. Blood in the urine (hematuria) may herald BPH, but most men with BPH do not have hematuria. Screening and Diagnosis The American Urological Association (AUA) Symptom Index provides an objective assessment of BPH symptoms that helps to decide on treatment. However, this index cannot be used for diagnosis, since other diseases can cause symptoms similar to those of BPH. A medical history will give clues to conditions that can mimic BPH, such as possible stricture, bladder cancer or stones, or abnormal bladder function (problems with holding or emptying urine) due to a neurologic disorder (neurogenic bladder). Strictures can result from urethral damage caused by prior trauma, instrumentation (for example, catheter insertion), or an infection, such as gonorrhea. Bladder cancer is suspected if there is a history of blood in the urine. Pain in the penis or bladder area may indicate bladder stones or infection. A neurogenic bladder is suggested when an individual has diabetes or a neurologic disease such as multiple sclerosis or Parkinson's disease, or describes a recent deterioration in sexual function. A thorough medical history should also include questions about previous urinary tract infections or prostatitis (inflammation of the prostate that may cause pain in to lower back and the area between the scrotum and rectum, chills, fever, and general malaise), and any worsening of urinary symptoms when taking cold or sinus drugs. The physician will also ask whether any over-the-counter or prescription medications are being taken, because certain varieties can make voiding symptoms worse in men with BPH. The physical examination may begin with the doctor observing urination to completion to detect any urinary irregularities. The doctor will manually examine the lower abdomen to check for the presence of a mass, which may indicate an enlarged bladder due to retained urine. In addition, a digital rectal exam (DRE) which allows the physician to assess the size, shape, and consistency of the prostate, is essential for proper diagnosis. This important examination involves the insertion of a gloved finger into the rectum, but is only mildly uncomfortable. The detection of hard or firm areas in the prostate raises the suspicion of prostate cancer. If the history suggests possible neurologic disease, the physical may also include an examination for neurological abnormalities that indicate the urinary symptoms result from a neurogenic bladder. A urinalysis, which is obtained in all patients with symptoms of BPH, may be the only laboratory test if symptoms are mild and no other abnormalities are suspected from the medical history and physical examination. A urine culture is added if a urinary infection is suspected. With more severe chronic symptoms of BPH, blood creatinine of blood urea nitrogen (BUN) and hemoglobin are measured to rule out kidney damage and anemia. Measuring prostate specific antigen (PSA) levels in the blood to screen for prostate cancer is recommended
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WHAT IS HYPERPROLACTINEMIA? Hyperprolactinemia is a condition of elevated serum prolactin. Prolactin is a 198-amino acid protein produced in the lactotroph cells of the anterior pituitary gland.....
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An action potential is a rapid rise and subsequent fall in voltage or membrane potential across a cellular membrane with a characteristic pattern. Sufficient current is required to initiate a voltage response in a cell membrane; if the current is insufficient to depolarize the membrane to the threshold level, an action potential will not fire The resting membrane potential is caused by the distribution of ions inside and outside the neurons. The inside of the cell contains large, negatively charged organic particles(e.g proteins). The movement of smaller positively and negatively charged inorganic molecules occurs only through special channels. The cell membrane also has active pumps that use energy to pump ions in and out; Therefore, at rest, the inside is maintained more negative than the outside. At rest, the inside of the neuron (intracellular fluid) has more potassium ions (K) and proteins (Pr ), and The outside has more sodium (Na) and chloride ions (Cl). because the cell membrane is not freely permeable to the ions. If it was, the ions would diffuse in and out to equalize the composition in and out of the cell. In this case, because of semi permeability, the ions only move in and out of the cell through CHANNELS on the cell membrane specific for each ion. MEMBRANE CHANNELS The cell membranes of nerves, like those of other cells, contain many different types of ion channels. Types of channels voltage-gated channels – are operated by changes in voltage. ligand-gated channels Operated by hormones and other chemicals These channels open when the chemical binds to receptor sites on the cell membrane. Mechanically-regulated channels – regulated mechanically At rest, there is a leak of sodium into the cell and potassium out of the cell. More potassium leaves the cell than sodium enters cell. This is one of the reasons why the inside of a nerve is negative at -70 mV. To combat the leak, a pump on the cell membrane, the sodium potassium (Na-K) pump or sodium-potassium ATPase, constantly pushes sodium out of the cell and brings potassium into the cell, using energy. PRODUCTION OF IMPULSES The neurons communicate with each other by changing the electrical potential inside the cell. This is achieved by movement of ions in and out of the cell and is determined by the permeability of the nerve cell membrane. Nerve cells have a low threshold for excitation. The stimulus may be electrical, chemical, or mechanical. Two types of physicochemical disturbances are produced: Local, non-propagated potentials Propagated disturbances, the action potentials (or nerve impulses). They are due to changes in the conduction of ions across the cell membrane that are produced by alterations in ion channels. ACTION POTENTIAL When a cell is stimulated, sodium channels open and sodium diffuses into the cell along its electrochemical gradient. The inside becomes less negative and this is known as DEPOLARIZATION. The stimuli are removed, the cell returns to its resting membrane potential Soon after original state and this is known as REPOLARIZATION When a neuron is sufficiently stimulated to depolarize it to a threshold value of about -60 to -55 mV. Many voltage-gated sodium channels are opened and sodium rushes in, further depolarizing the cell. This depolarization is rapid and propagated throughout the cell along the axon. An action potential or nerve impulse is a rapid change in potential that is propagated along the cell. The direction of propagation of action potentials is from the dendrite or cell body down an axon. As a result of opening and closing of other voltage gated channels, the depolarization does not last long and the cell is repolarized to reach its original resting potential. The voltage-gated sodium channels close when the potential becomes more and more positive. At the same time, voltage-gated potassium channels open and potassium rushes out repolarizing the cell A decrease in extracellular Ca2+ concentration increases the excitability of nerve and muscle cells by decreasing the amount of depolarization necessary to initiate the changes in the Na+ and K+ conductance that produce the action potential. Conversely, an increase in extracellular Ca2+ concentration "stabilizes the membrane" by decreasing excitability.
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Renin Angiotensin Aldosterone system (RAAS)
The renin–angiotensin-Aldosterone system (RAS) or the renin–angiotensin–aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance. In this video you will learn on the interplay of these hormones ...
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Gram-positive bacteria are bacteria that give a positive result in the Gram stain test, which is traditionally used to quickly classify bacteria into two broad categories according to their cell wall. Gram-positive bacteria take up the crystal violet stain used in the test, and then appear to be purple-coloured when seen through a microscope. This is because the thick peptidoglycan layer in the bacterial cell wall retains the stain after it is washed away from the rest of the sample, in the decolorization stage of the test. Gram-negative bacteria cannot retain the violet stain after the decolorization step; alcohol used in this stage degrades the outer membrane of gram-negative cells, making the cell wall more porous and incapable of retaining the crystal violet stain. Their peptidoglycan layer is much thinner and sandwiched between an inner cell membrane and a bacterial outer membrane, causing them to take up the counterstain (safranin or fuchsine) and appear red or pink. Despite their thicker peptidoglycan layer, gram-positive bacteria are more receptive to certain cell wall targeting antibiotics than gram-negative bacteria, due to the absence of the outer membrane , the following characteristics are present in gram-positive bacteria: Cytoplasmic lipid membrane Thick peptidoglycan layer Teichoic acids and lipoids are present, forming lipoteichoic acids, which serve as chelating agents, and also for certain types of adherence. Peptidoglycan chains are cross-linked to form rigid cell walls by a bacterial enzyme DD-transpeptidase. A much smaller volume of periplasm than that in gram-negative bacteria. Gram positive cells have two layers- inner cytoplasmic membrane and outer thick peptidoglycan Whereas gram negative cells have three layers-inner cytoplasmic membrane, thin peptidoglycan layer and outer membrane with lipopolysaccharide Gram positive have low lipid content while gram negative have high lipid content Gram positive have no endotoxins while gram negative have endotoxin-lipid A Gram positive have no porins while gram negative have porin channels Gram positive are vulnerable to lysozyme and penicillin attack while gram negative are resistant to lysozyme and penicillin attack
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Caesarean section, also known as C-section, or caesarean delivery, is the use of surgery to deliver babies. A caesarean section is often necessary when a vaginal delivery would put the baby or mother at risk. This may include obstructed labour, twin pregnancy, high blood pressure in the mother, breech birth, or problems with the placenta or umbilical cord. A caesarean delivery may be performed based upon the shape of the mother's pelvis or history of a previous C-section. A trial of vaginal birth after C-section may be possible. The World Health Organization recommends that Caesarean section be performed only when medically necessary. Some C-sections are performed without a medical reason, upon request by someone, usually the mother. A C-section typically takes 45 minutes to an hour. It may be done with a spinal block, where the woman is awake or under general anesthesia. A urinary catheter is used to drain the bladder and the skin of the abdomen is then cleaned with an antiseptic. An incision of about 15 cm (6 inches) is then typically made through the mother's lower abdomen. The uterus is then opened with a second incision and the baby delivered. The incisions are then stitched closed. A woman can typically begin breastfeeding as soon as she is awake and out of the operating room. Often, several days are required in the hospital to recover sufficiently to return home. C-sections result in a small overall increase in poor outcomes in low-risk pregnancies. They also typically take longer to heal from, about six weeks, than vaginal birth. The increased risks include breathing problems in the baby and amniotic fluid embolism and postpartum bleeding in the mother. Established guidelines recommend that caesarean sections not be used before 39 weeks of pregnancy without a medical reason. The method of delivery does not appear to have an effect on subsequent sexual function
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